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The Coming Plague

Page 97

by Laurie Garrett

Viewing footage of the old cow town transported the retired physician back to a time when he was a strapping, though naïve, physician in Sausalito, California. And to that day in 1962 in La Paz when the Bolivian Minister of Health asked if he would mind taking a look at a mysterious typho negro outbreak deep in the Bolivian interior.

  MacKenzie sat in his living room for a few moments, recalling the terror that struck Bolivia’s Machupo River region when the strange hemorrhagic fever swept through. And he wondered how, after the passage of thirty years, the people had fared.

  He reached for his telephone and called Montana. Karl Johnson, also long retired and living the way he preferred, in rugged cowboy country surrounded by prime trout-fishing streams, answered the phone. The old colleagues resolved to revisit San Joaquín.

  MacKenzie, recalling the difficulties involved in reaching the remote area during the 1960s, called a colleague in La Paz for transportation advice, and made arrangements for a September trip. MacKenzie told the colleague that he and Johnson just wanted to have a little look-see after all these years.

  For several months a new outbreak of Bolivian hemorrhagic fever had been raging in areas near San Joaquín, and CDC investigators had assisted the government in proving that the Machupo virus had made a comeback. Once again, for the first time in thirty years, Bolivia was waging an aggressive mouse control campaign in the region. That, too, piqued Johnson and MacKenzie’s interest.

  When the Americans arrived in La Paz, they were surprised by their warm, high-level reception. Thirty years was a long time—neither of them expected anyone to remember their efforts so long ago in the remote savanna region. But ceremonies, praise, and medals were lavished on the stunned scientists during their days in the capital—so much so that their journey to San Joaquín was delayed by nearly forty-eight hours.

  Finally, the government arranged for a plane to fly the pair of scientists to the remote region, and MacKenzie reexperienced the dizzying ascent from the mile-high city, the passage through the Andes, and the descent into the steamy headlands of the Amazon.

  As the plane approached San Joaquín, Johnson and MacKenzie wondered what was going on: there seemed to be quite a crowd gathered around the airstrip. When they landed, MacKenzie asked if their trip might be coinciding with the arrival of some dignitary or politician.

  The moment they stepped out of the aircraft, a local marching band struck up a stirring tune and more than 300 peasants, cowboys, children, and farmers cheered the Americans. MacKenzie and Johnson were overwhelmed by the exuberant, joyous crowd, the hugs and handshakes, the flowers and gifts. Neither man could believe that the people of San Joaquín recognized them, or remembered their search, so long ago, for the source of Bolivia’s plague.

  “Most of these people weren’t even alive back then,” MacKenzie said to Johnson, who shared his sense of amazement.

  But for the people of San Joaquín the names of MacKenzie, Kuns, Johnson, and Webb were emblazoned permanently on their cultural memory. Streets, some of which were now paved, were named after the near-mythic heroes from North America who had spared San Joaquín from doom. Even the schoolchildren knew who the white-haired “disease cowboys” were.

  These were the men who stopped their plague.

  And that was why for more than forty-eight hours the people of San Joaquín had waited patiently through the intermittent rain, standing on the landing strip and staring hopefully into the western sky.

  Notes

  Introduction

  1 R. M. Krause. Washington, D.C.: National Foundation for Infectious Diseases, 1981.

  2 R. M. Krause, Foreword to S. S. Morse, ed., Emerging Viruses (Oxford, Eng.: Oxford University Press, 1993).

  3 J. Lederberg, R. E. Shope, and S. C. Oaks, Jr., Washington, D.C.: National Academy Press, 1992.

  4 E. O. Wilson, The Diversity of Life (Cambridge, MA: Harvard University Press, 1992). 31.

  5 A. Gore, Earth in the Balance (New York: Houghton Mifflin, 1992).

  6 J. Lederberg, “Medical Science, Infectious Disease, and the Unity of Mankind,” Journal of the American Medical Association 260 (1988): 684–85; and Institute of Medicine, Emerging Infections: Microbial Threats to Health in the United States (Washington, D.C.: National Academy Press. 1992).

  1. Machupo

  1 K. M. Johnson, et al., “Virus Isolations from Human Cases of Hemorrhagic Fever in Bolivia.” Proceedings of the Society of Experimental Biology and Medicine 118 (1965): 113–18.

  2 H. W. Lee, “Korean Hemorrhagic Fever,” in S. R. Pattyn, ed., Ebola Virus Hemorrhagic-Fever (Amsterdam: Elsevier Press, 1978), 331–43.

  3 R. G. Gordon, et al., “Bolivian Hemorrhagic Fever Probably Transmitted by Personal Contact,” American Journal of Epidemiology 82 (1965): 85–91.

  4 Several years later Kuns would toil over insect samples he collected in San Joaquín and discover that a species of soft tick. Ornithodoros boliviensis, carried a virus. It was not, however, the virus responsible for the human epidemic. Nor did it match any other type of South American virus. So Kuns dubbed his new microbe Matucare virus, after a stream near San Joaquín. He showed the virus was lethal for baby mice and guinea pigs but harmless to human beings. Matucare virus would never have been discovered had there not been a human disease outbreak near the habitat of the 0. boliviensis tick.

  5 R. B. MacKenzie, P. A. Webb, and K. M. Johnson, “Detection of Complement-Fixing Antibody After Bolivian Hemorrhagic Fever, Employing Machupo, Junín and Tacaribe Virus Antigen,” American Journal of Tropical Medicine and Hygiene 14 (1965): 1079–84; K. M. Johnson et al.. “Isolation of Machupo Virus from Wild Rodent Calomys callosus,” American Journal of Tropical Medicine and Hygiene 15 (1966): 103–6; P. A. Webb, “Properties of Machupo Virus,” American Journal of Tropical Medicine and Hygiene 14 (1965): 799–801; P. A. Webb et al., “Some Characteristics of Machupo Virus. Causative Agent of Bolivian Hemorrhagic Fever,” American Journal of Tropical Medicine and Hygiene 16 (1967): 531–38; and K. M. Johnson, “Arenaviruses,” in B. N. Fields et al., eds., Virology (New York: Raven Press, 1985), 1033–53.

  The U.S. Army provided logistical support to the ongoing Machupo investigation. In 1964 a Sergeant Lowery got infected and very nearly died of the disease. As had Webb months earlier. Lowery’s wife comforted the ailing sergeant and also developed the disease. Lowery’s condition was so severe that one Sunday morning the hospital director ordered the Gorgas pathologist put on standby to perform an autopsy. Meanwhile. MacKenzie gave Lowery a pint of his blood, hoping it contained helpful antibodies. Whether or not the antiserum made the difference will never be known, but later that Sunday Lowery started to recover. The sergeant and his wife survived Machupo.

  6 A. S. Parodi, et al., “Sobre la Etiologia del Brote Epidémico de Junín,” Día Médica 30 (1958): 2300–1.

  Jordi Casals, of the Rockefeller Foundation, isolated the actual virus for Junín disease. He discovered it closely resembled another mouse virus called LCM (lymphocytic choriomeningitis virus), which he had accidentally stumbled upon in 1958 while studying rabies-infected mouse cells. Casals dubbed LCM. and later Junín. Tacaribe, and Machupo, “arenaviruses” because under high-powered microscopes tissues infected with these agents “looked as though they had been sprinkled with sand.” The word “arena” is Latin for sand. In 1964 Casals isolated another new arenavirus from Brazilian mice, dubbed Ampari virus. Fortunately. Ampari proved harmless to human beings. N. Mettler, S. M. Buckley, and J. Casals, “Propagation of Junín Virus, the Etiological Agent of Argentine Hemorrhagic Fever, in HeLa Cell Cultures,” Proceedings of the Society of Experimental Biology and Medicine 107 (1961): 684–88: and F. P. Pinheiro et al., “Amapari, a New Virus of the Tacaribe Group from Rodents and Mites of Amapa Territory, Brazil,” Proc
eedings of the Society of Experimental Biology and Medicine 122 (1966): 531–35.

  7 Knowing the cause of a disease, even a terrible hemorrhagic one, is only the first step. Despite such knowledge, over 20,000 people have suffered acute Junín since its 1958 discovery, and the territory of the virus-carrying mouse has steadily expanded from the Buenos Aires province to, by 1985. three neighboring provinces of Argentina. Case fatality rates in recent outbreaks have been as high as 30 percent of all infected people. After Johnson and his colleagues completed their Machupo work in San Joaquín, another outbreak of that disease occurred in Beni, Bolivia, some years later. See World Health Organization. “Viral Haemorrhagic Fevers: Report of a WHO Expert Committee,” Technical Report Series 721 (1985).

  8 In 1972 Machupo broke out again in an area about forty miles from San Joaquín. Though details of exactly how the epidemic began remained elusive. Kuns’s investigations pointed to the daughter of a wealthy ranchero owner. She apparently got Machupo after visiting her boyfriend, a young man from the village of Magdalena. Magdalena was the first Machupo-plagued town MacKenzie visited nine years earlier, and Kuns has always been convinced the ranchero owner’s daughter got infected through sexual contact with a person carrying the virus. Sadly, none of the published accounts of Machupo directly stated the possibility that the virus could be transmitted through sexual intercourse, although official accounts of Webb’s illness spelled out the likelihood Machupo could be passed from person to person by a kiss.

  9 “The Search for the Invisible Killer,” Saturday Evening Post, December 3, 1966: 92–96.

  2. Health Transition

  1 A. R. Hinman et al., “Live or Inactivated Poliomyelitis Vaccine: An Analysis of Benefits and Risks.” American Journal of Public Health 78 (1988): 291–95.

  2 J. A. Najera, “Malaria and the Work of WHO,” Bulletin of the World Health Organization 67 (1989): 229–43.

  3 Ibid.

  4 J. S. Horn, “Away with All Pests”: An English Surgeon in People’s China: 1954–1969 (London: Modern Reader, 1969).

  5 Schistosomiasis is a deadly intestinal and liver disease caused by parasitic worms. The disease process begins when adult snails insert worm eggs into the bloodstream of a human being who works or plays along the edges of canals, streams, irrigation ditches, or lakes. The eggs grow, becoming worms, or flukes, that reside in the liver.

  6 Horn (1969), op. cit.

  7 U.S. Department of Health. Education, and Welfare. Selected Disease Control Programs (Washington, D.C., 1966).

  8 U.S. Department of Health, Education, and Welfare. Study Group on the Mission and Organization of the Public Health Service: Final Report (Washington. D.C., 1960).

  9 W. H. Stewart, “A Mandate for State Action,” presented at the Association of State and Territorial Health Officers, Washington. D.C.. December 4, 1967.

  10 J. Lederberg et al., Emerging Infections: Microbial Threats to Health in the United States (Washington. D.C.: National Academy Press, 1992).

  11 Further information can be found in: J. D. Watson et al., Molecular Biology of the Gene (4th ed.; Menlo Park. CA: The Benjamin/Cummings Publishing Company, 1987); P. Berg and M. Singer, Dealing with Genes: The Language of Heredity (Mill Valley, CA: University Science Books, 1992); and J. D. Watson, The Double Helix (New York: New American Library, 1969).

  12 F. J. Fenner et al., The Biology of Animal Viruses (New York: Academic Press, 1968).

  13 For excellent renditions of the history of antibiotics and controversies concerning the rise of bacterial resistance to the chemicals, the reader is referred to two highly readable books: M. Lappé, Germs That Won’t Die (Garden City, NY: Anchor Press, 1982); and S. B. Levy. The Antibiotic Paradox (New York: Plenum Press, 1992).

  14 J. Lederberg and E. M. Lederberg, “Replica Plating and Indirect Selection,” Journal of Bacteriology 63 (1952): 399–406.

  15 Webster’s New Twentieth Century Dictionary Unabridged (New York: Collins World, 1975).

  16 J. Farley, “Parasites and the Germ Theory of Disease,” in Framing Disease, eds. C. E. Rosenberg and J. Golden (New Brunswick, NJ: Rutgers University Press, 1992), 33–49.

  17 Among the monkey species known to serve as malaria reservoirs in Africa, Asia, and South America are P. knowlesi, P. cynomolgi, P. brasilianum, P. invi, P. scwetzi, and P. simium.

  18 Two well-organized, excellent texts provide a quick thumbnail description of all infectious diseases prominent on the planet at this time. Both provide basic information on the hosts, reservoirs, and life cycles of parasites. The reader is referred to A. S. Benenson, ed., Control of Communicable Diseases in Man (15th ed.; Washington, D.C.: American Public Health Association, 1990); and M. E. Wilson, A World Guide to Infections: Diseases, Distribution, Diagnosis (Oxford, Eng.: Oxford University Press, 1991).

  19 T. McKeown, The Origins of Human Disease (Oxford, Eng.: Basil Blackwell, 1988), 52.

  20 W. H. McNeill, Plagues and Peoples (New York: Doubleday, 1976), 103.

  21 F. Fenner, D. A. Henderson, I. Arita, et al., Smallpox and Its Eradication (Geneva: World Health Organization, 1988).

  22 Smallpox is a relatively recent human disease, seeming to have arisen in India less than 2,000 years ago. In ancient times medical observers could not clearly discriminate between smallpox and other human-to-human epidemic diseases such as measles, bubonic plague, and typhus. As a result, controversy reigns over modern interpretations of ancient medical records.

  Nevertheless, several major epidemics that claimed a quarter to a third of the affected populations were, according to historians familiar with medical records, likely to have been smallpox. These include:

  Epidemic Site Year

  China A.D. 49

  Rome 165

  Cyprus 251–66

  Greece 312

  Japan 552

  Mecca 569–71

  Arabia 683

  Europe, various sites 700–800

  Compiled from A. Patrick, “Diseases in Antiquity: Ancient Greece and Rome,” in D. Brothwell and A. T. Sandison, eds., Diseases in Antiquity (Springfield. IL: Charles C Thomas, 1967), 238–46; R. Hare, “The Antiquity of Diseases Caused by Bacteria and Viruses: A Review of the Problem from a Bacteriologist’s Point of View,” ibid., 115–31; and McNeill (1977), op. cit., 2, 103, 118, 124.

  23 W. M. Denevan, The Native Population of the Americas in 1492 (Madison: University of Wisconsin Press, 1992).

  Smallpox may have been the most useful weapon of biological warfare in world history. European colonialists repeatedly took advantage of the special susceptibility of the Amerindian population, deliberately spreading the deadly virus among Indians who were successfully defending their rights to the lands and resources of the Americas. For example, in 1763 Sir Jeffrey Amherst, commander in chief of all British forces in North America, was having great difficulty controlling the Pontiac Indians in the western territories. At Amherst’s insistence, blankets inoculated with live smallpox viruses were distributed to the Pontiac, obliterating the tribe. The deliberately induced epidemic quickly spread to the northwest, claiming large numbers of Sioux and Plains Indians, crossed the Rookies and inflicted huge death tolls among Native Americans from southern California all the way north to the Arctic Circle tribes of Alaska. This devastation was cited in the official WHO history of smallpox: Fenner, Henderson, Arita, et al., (1988), op. cit.

  24 Fenner, Henderson, Arita, et al. (1988), op. cit.

  25 English physician Edward Jenner discovered in 1796 that cowpox, which was harmless to people, could be used as a vaccine against smallpox. The riskier idea of inoculating people with small amounts of human smallpox to raise immunity goes back in some cultures to ancient times, although some people developed the disease after injection. The British royal family was so immunized in 1722, as was the entire American Revolutionary Army under
the command of General George Washington in 1776.

  26 Spectacular accounts of the smallpox campaign can be found in June Goodfield’s Quest for Killers (Boston: Birkhauser, 1985), 191–244; and Horace G. Ogden’s CDC and the Smallpox Crusade, HHS Publication No. (CDC)87–8400 (Washington, D.C.: U.S. Government Printing Office, 1987).

  27 In Ghana, for example, there were at least six major smallpox epidemics between 1901 and 1960, and in some the mortality rate among those infected with the virus was a staggering 50 percent. Whole villages were decimated, and the disease disrupted the national economy. Yet in no year were more than 1,950 cases registered in federal records. See D. Scott, Epidemic Disease in Ghana 1901–1960 (London: Oxford University Press, 1965), 65–84.

  28 In 1978 two people in Birmingham, England, contracted smallpox as a result of a laboratory accident. The Birmingham laboratory illegally possessed smallpox samples, and lab photographer Janet Parker died as a result of a containment failure. Her mother also was infected, but survived. Today samples of the two types of smallpox exist in just two high-security laboratories: the CDC’s Atlanta lab and a Moscow facility. The CDC is currently sequencing the entire genetic code of the more dangerous variola major virus. And Moscow scientists are sequencing the less lethal variola minor form. By international agreement, both the Atlanta and Moscow smallpox samples are scheduled to be destroyed when gene sequencing is complete, although the elimination of all surviving viruses is a matter of considerable controversy.

 

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